The effects of TNF-α inhibitors on carbon tetrachloride-induced nephrotoxicity

Carbon tetrachloride (CCl₄), employed in various industrial fields, can cause acute damage in renal tissues. This study investigated the therapeutic effect of the TNF-alpha inhibitor Infliximab on TGF-ß and apoptosis caused by acute kidney image induced by CCl₄.

Twenty-four male Sprague-Dawley rats were assigned into control, CCl₄, and CCl₄+ Infliximab groups. The control group received an isotonic saline solution, and the CCl₄ group 2 mL/kg CCl₄ intraperitoneally (i.p). The CCl₄+ Infliximab group was given 7 mg/kg Infliximab 24 hours after administration of 2 mL/kg CCl₄. Kidney tissues were removed at the end of the experiment and subjected to histopathological and biochemical analysis.

The application of CCl₄ led to tubular necrosis, inflammation, vascular congestion, and increased Serum BUN and creatinine values. An increase in caspase-3 activity also occurred in the CCl₄ group. However, Infliximab exhibited an ameliorating effect on kidney injury by causing a decrease in the number of apoptotic cells. Tissue ADA and TGF-ß values of the CCL4 group were significantly higher than the values of the control group (p = .001, p < .001 respectively) and CCL₄+ Inf group (p = .004, p = .015, respectively).

This study shows that Infliximab ameliorates nephrotoxicity by reducing lipid peroxidation, oxidative stress, and apoptosis in acute kidney damage developing in association with CCl₄ administration. These findings are promising in terms of the ameliorating role of TNF-alpha inhibitors in acute kidney injury.